Cyclin D–CDK4 kinase destabilizes PD-L1 via cullin 3–SPOP to control cancer immune surveillance

Jinfang Zhang, Xia Bu, Haizhen Wang, Yasheng Zhu, Yan Geng, Naoe Taira Nihira, Yuyong Tan, Yanpeng Ci, Fei Wu, Xiangpeng Dai, Jianping Guo, Yu-Han Huang, Caoqi Fan, Shancheng Ren, Yinghao Sun, Gordon J. Freeman (), Piotr Sicinski () and Wenyi Wei ()
Additional contact information
Jinfang Zhang: Beth Israel Deaconess Medical Center, Harvard Medical School
Xia Bu: Dana-Farber Cancer Institute, Harvard Medical School
Haizhen Wang: Harvard Medical School
Yasheng Zhu: Shanghai Changhai Hospital, Second Military Medical University
Yan Geng: Harvard Medical School
Naoe Taira Nihira: Beth Israel Deaconess Medical Center, Harvard Medical School
Yuyong Tan: Beth Israel Deaconess Medical Center, Harvard Medical School
Yanpeng Ci: Beth Israel Deaconess Medical Center, Harvard Medical School
Fei Wu: Beth Israel Deaconess Medical Center, Harvard Medical School
Xiangpeng Dai: Beth Israel Deaconess Medical Center, Harvard Medical School
Jianping Guo: Beth Israel Deaconess Medical Center, Harvard Medical School
Yu-Han Huang: Beth Israel Deaconess Medical Center, Harvard Medical School
Caoqi Fan: Harvard Medical School
Shancheng Ren: Shanghai Changhai Hospital, Second Military Medical University
Yinghao Sun: Shanghai Changhai Hospital, Second Military Medical University
Gordon J. Freeman: Dana-Farber Cancer Institute, Harvard Medical School
Piotr Sicinski: Harvard Medical School
Wenyi Wei: Beth Israel Deaconess Medical Center, Harvard Medical School

Nature, 2018, vol. 553, issue 7686, 91-95

Abstract: Abundance of PD-L1, the ligand of the anti-cancer immunotherapy target PD-1, is negatively regulated by poly-ubiquitination via the cyclin D–CDK4/cullin 3–SPOP axis and PD-1 blockade treatment in mice improved survival when combined with CDK4/6 inhibitors.

Date: 2018
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DOI: 10.1038/nature25015

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